引自Harrison's Principles of Internal Medicine, 19e chap. 300: Deep Venous Thrombosis and Pulmonary Thromboembolism
某次內專有考這一題,pulmonary embolism的機轉:
- 最常見的氣體交換異常是 (1) arterial hypoxeima與 (2) A-a gradient變大。(→表示 O2無法有效進入肺部)
- 解剖性死腔(Anatomic dead space)增加 ←氣無法吸入;生理性死腔(Physiologic dead space)增加 ← 過多靜脈血流到肺微血管
- 其他異常:
- 肺血管阻力增加,由於血管阻塞或血小板分泌的vasoconstricting neurohumoral agents (如serotonin);血栓塞住的遠端會釋放vasoactive mediators,會造成 ventilation-perfusion mismatching,如此一來可以解釋discordance between a small PE and a large alveolar-arterial O2 gradient (小小的阻塞就會造成很大的A-a gradient)
- 氣體交換異常,由於 a. (vascular obstruction→) alveolar dead space增加, b. hypoxemia (← alveolar hypoventilation,相對於nonobstructed lung的perfusion), c. right-to-left shunting, d. impaired carbon monoxide transfer due to loss of gas exchange surface.
- Alveolar hyperventilation (← reflex stimulation of irritant receptors)
- airway resistance 上升 (因為constriction of airways distal to the bronchi)
- pulmonary compliance 下降 (因為lung edema, lung hemorrhage, or loss of surfactant)
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